Suv39h1 downregulation inhibits neointimal hyperplasia after vascular injury. 2019

Jing Zhang, and Jing Chen, and Jun Yang, and Changwu Xu, and Qi Hu, and Hui Wu, and Wanyin Cai, and Qing Guo, and Wenqi Gao, and Chao He, and Chaojun Yang, and Jian Yang
Central Laboratory, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, 443003, China; Department of Cardiology, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, 443003, China.

Neointimal hyperplasia resulting from pathological vascular smooth muscle cells (VSMCs) activation is a common pathophysiological basis for numerous proliferative vascular diseases, such as restenosis. Suv39h1, an important transcription suppressor, may be involved in this process. Herein, we investigated the role of Suv39h1 in pathological intimal hyperplasia and its possible mechanisms in vitro and in vivo. An adenovirus vector for Suv39h1 overexpression and a lentiviral vector for its downregulation were constructed and used to transfect cultured VSMCs in vitro. The functional changes in VSMCs stimulated by angiotensin II (Ang II) were observed and the possible mechanism was investigated. Additionally, rat carotid arteries with balloon injury were locally transfected with these viral vectors and changes in neointima formation, proliferating cell nuclear antigen (Pcna) expression and collagen deposition were examined. Upon Ang II stimulation, the expression of Suv39h1 and inhibitor of DNA binding 3 (Id3) was significantly increased. Suv39h1 downregulation inhibited Ang II-stimulated migration and proliferation of VSMCs, antagonized the production of Id3 and promoted p21 and p27Kip1 expression. In contrast, Suv39h1 overexpression had the opposite effects. Suv39h1 regulated the transcription of p21 and p27Kip1 by controlling H3K9me3 in the proximal promoter regions. Consistent with the VSMCs results, Suv39h1 and Id3 expression was significantly increased in blood vessels after balloon injury. Suv39h1 downregulation inhibited intimal hyperplasia, and attenuated Pcna expression and collagen synthesis in the intima, while Suv39h1 overexpression had the opposite effects. Suv39h1 downregulation effectively inhibited neointimal hyperplasia after vascular injury.

UI MeSH Term Description Entries
D006965 Hyperplasia An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells. Hyperplasias
D008297 Male Males
D008780 Methyltransferases A subclass of enzymes of the transferase class that catalyze the transfer of a methyl group from one compound to another. (Dorland, 28th ed) EC 2.1.1. Methyltransferase
D009131 Muscle, Smooth, Vascular The nonstriated involuntary muscle tissue of blood vessels. Vascular Smooth Muscle,Muscle, Vascular Smooth,Muscles, Vascular Smooth,Smooth Muscle, Vascular,Smooth Muscles, Vascular,Vascular Smooth Muscles
D012097 Repressor Proteins Proteins which maintain the transcriptional quiescence of specific GENES or OPERONS. Classical repressor proteins are DNA-binding proteins that are normally bound to the OPERATOR REGION of an operon, or the ENHANCER SEQUENCES of a gene until a signal occurs that causes their release. Repressor Molecules,Transcriptional Silencing Factors,Proteins, Repressor,Silencing Factors, Transcriptional
D002465 Cell Movement The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell. Cell Migration,Locomotion, Cell,Migration, Cell,Motility, Cell,Movement, Cell,Cell Locomotion,Cell Motility,Cell Movements,Movements, Cell
D002478 Cells, Cultured Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others. Cultured Cells,Cell, Cultured,Cultured Cell
D004195 Disease Models, Animal Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases. Animal Disease Model,Animal Disease Models,Disease Model, Animal
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D015398 Signal Transduction The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. Cell Signaling,Receptor-Mediated Signal Transduction,Signal Pathways,Receptor Mediated Signal Transduction,Signal Transduction Pathways,Signal Transduction Systems,Pathway, Signal,Pathway, Signal Transduction,Pathways, Signal,Pathways, Signal Transduction,Receptor-Mediated Signal Transductions,Signal Pathway,Signal Transduction Pathway,Signal Transduction System,Signal Transduction, Receptor-Mediated,Signal Transductions,Signal Transductions, Receptor-Mediated,System, Signal Transduction,Systems, Signal Transduction,Transduction, Signal,Transductions, Signal

Related Publications

Jing Zhang, and Jing Chen, and Jun Yang, and Changwu Xu, and Qi Hu, and Hui Wu, and Wanyin Cai, and Qing Guo, and Wenqi Gao, and Chao He, and Chaojun Yang, and Jian Yang
January 2009, Journal of vascular research,
Jing Zhang, and Jing Chen, and Jun Yang, and Changwu Xu, and Qi Hu, and Hui Wu, and Wanyin Cai, and Qing Guo, and Wenqi Gao, and Chao He, and Chaojun Yang, and Jian Yang
January 2009, Journal of atherosclerosis and thrombosis,
Jing Zhang, and Jing Chen, and Jun Yang, and Changwu Xu, and Qi Hu, and Hui Wu, and Wanyin Cai, and Qing Guo, and Wenqi Gao, and Chao He, and Chaojun Yang, and Jian Yang
April 2000, Journal of cardiovascular pharmacology,
Jing Zhang, and Jing Chen, and Jun Yang, and Changwu Xu, and Qi Hu, and Hui Wu, and Wanyin Cai, and Qing Guo, and Wenqi Gao, and Chao He, and Chaojun Yang, and Jian Yang
January 2019, EBioMedicine,
Jing Zhang, and Jing Chen, and Jun Yang, and Changwu Xu, and Qi Hu, and Hui Wu, and Wanyin Cai, and Qing Guo, and Wenqi Gao, and Chao He, and Chaojun Yang, and Jian Yang
May 2004, Journal of vascular surgery,
Jing Zhang, and Jing Chen, and Jun Yang, and Changwu Xu, and Qi Hu, and Hui Wu, and Wanyin Cai, and Qing Guo, and Wenqi Gao, and Chao He, and Chaojun Yang, and Jian Yang
February 1994, Stroke,
Jing Zhang, and Jing Chen, and Jun Yang, and Changwu Xu, and Qi Hu, and Hui Wu, and Wanyin Cai, and Qing Guo, and Wenqi Gao, and Chao He, and Chaojun Yang, and Jian Yang
May 2023, Kardiologiia,
Jing Zhang, and Jing Chen, and Jun Yang, and Changwu Xu, and Qi Hu, and Hui Wu, and Wanyin Cai, and Qing Guo, and Wenqi Gao, and Chao He, and Chaojun Yang, and Jian Yang
December 2000, The American journal of pathology,
Jing Zhang, and Jing Chen, and Jun Yang, and Changwu Xu, and Qi Hu, and Hui Wu, and Wanyin Cai, and Qing Guo, and Wenqi Gao, and Chao He, and Chaojun Yang, and Jian Yang
January 2022, Journal of radiation research,
Jing Zhang, and Jing Chen, and Jun Yang, and Changwu Xu, and Qi Hu, and Hui Wu, and Wanyin Cai, and Qing Guo, and Wenqi Gao, and Chao He, and Chaojun Yang, and Jian Yang
November 2008, Circulation journal : official journal of the Japanese Circulation Society,
Copied contents to your clipboard!